Chickenpox is caused by varicella-zoster virus (VZV), a member of the herpesvirus group. The disease occurs in persons with no prior VZV immunity. VZV-specific antibodies can be demonstrated shortly after onset of disease, decline during convalesence, but remain detectable for many years and correlate with immunity to the disease. Chickenpox is highly contagious; over 90% of the population becomes exposed to VZV during the first two decades. The disease is highly morbid to the immunosuppressed and to those beyond the second decade. In most, if not all cases, VZV becomes latent in dorsal root ganglion cells. From this latent state, VZV can reactivate and cause zoster even in the presence of specific antibodies, probably as a result of weakened cellular immunity.
VZV has six major glycoproteins on its surface: gp105, gp92, gp83, gp62, gp57, gp55. These glycoproteins apparently are the products of three genes: gA (gp105), gB (gp62, gp57) and gC (gp92, gp83, gp55). The gC glycoproteins are the majority and most immunogenic VZV glycoproteins. Some monoclonal antibodies to gA and gB display complement-independent neutralization, and monoclonal antibodies to gC display complement-dependent neutralization.